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Pharmaceutical Biology 2012-Jul

Inhaled essential oil from Chamaecyparis obtuse ameliorates the impairments of cognitive function induced by injection of β-amyloid in rats.

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Prisijungti Registracija
Nuoroda įrašoma į mainų sritį
Donghyuck Bae
Heejin Seol
Ho-Geun Yoon
Ju-Ryun Na
Kyonyeo Oh
Chul Yung Choi
Dong-wook Lee
Woojin Jun
Kwang Youl Lee
Jeongmin Lee

Raktažodžiai

Santrauka

BACKGROUND

Chamaecyparis obtusa Sieb. & Zucc., Endlicher (Cupressaceae) forest bathing or aromatherapy has been shown in various studies to have biological functions such as anticancer, antiallergies, antiinflammatory, and antioxidant activity. However, no reports exist on the pharmacological or biological activities of the essential oil of C. obtusa (EOCO) or its effects on central nervous system.

OBJECTIVE

The aggregation and formation of β-amyloid peptides (Aβ) into fibrils are central events in the pathogenesis of Alzheimer's disease (AD), and overproduction and aggregation of Aβ into oligomers have been known to trigger neurotoxicity. In this study, we investigated the effects of inhaled EOCO on cognitive function and neuronal apoptosis in rats intrahippocampally injected with Aβ.

METHODS

To model AD, 4 μg of aggregated Aβ was injected into the hippocampus. To test the effects of EOCO, behavioral performance in the Morris water maze was tested 4 days after injection. After behavioral testing, brain sections were prepared for TTC staining and TUNEL assay.

RESULTS

Inhaled EOCO protected spatial learning and memory from the impairments induced by Aβ(1-40) injection. In addition, the behavioral deficits accompanying Aβ(1-40)-induced AD were attenuated by inhalation of EOCO. Furthermore, acetylcholinesterase (AChE) activity and neuronal apoptosis were significantly inhibited in rats treated with Aβ(1-40) and EOCO compared to rats treated only with Aβ(1-40).

CONCLUSIONS

EOCO suppressed both AD-related neuronal cell apoptosis and AD-related dysfunction of the memory system. Thus, the results of this study support EOCO as a candidate drug for the treatment of AD.

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